tbuckley/cabot-search huggingface dataset:
Elevated Incidence of Childhood Leukemia in Woburn, Massachusetts: NIEHS Superfund Basic Research Program Searches for Causes
Authors: John L. Durant, Jia Chen, Harold F. Hemond, William G. Thilly
Journal: Environmental Health Perspectives (1995)

Between 1966 and 1986, the childhood leukemia rate in Woburn, Massachusetts, was 4-fold higher than the national average.A multidisciplinary research team from MIT, which is being supported by the NIEHS Superfund Basic Research Program, has explored the possible importance of a temporal correlation between the period of elevated leukemia and a previously unrecognized mobilization of toxic metals from a waste disposal site in north Woburn.Residents of Woburn may have been exposed to arsenic (70 pg/I) and chromium (240 pgAl at levels in excess of federal drinking water standards (50 pg/I for each metal) by consuming municipal groundwater contaminated with these metals.Research is currently underway a) to elucidate the mechanisms and the pathways by which these metals were transported from the waste disposal site to the drinking water supply; b) to determine the identity of the principal human cell mutagens in samples of aquifer materials collected from the site of the municipal supply wells; and c) to measure the extent of exposure and genetic change in residents who consumed the contaminated well water.
Abstract P184: Novel SCN5A Mutations and SNP in Patients with Brugada Syndrome
Authors: Kazufumi Nakamura, Daiji Miura, Kaoru Kobayashi, Mamoru Ouchida, Kenji Shimizu, Iori Ohmori, Nobuhiro Nishii, Satoshi Nagase, Hiroshi Morita, Yoshiki Hata, Takefumi Oka, Kengo Kusano, Tohru Ohe
Journal: Circulation (2008)

Background: Sodium channel alpha 5 subunit (SCN5A) mutations are important genetic abnormalities of Brugada syndrome (BS). Here we report novel SCN5A mutations in patients with BS. Methods and Results: Genomic mutations in the SCN5A gene were analyzed by PCR and direct sequencing in 121 patients with BS (119 men and 2 women). Thirteen (11%) of the patients had SCN5A mutation and five (4%) of the patients had single nucleotide polymorphisms (SNP) associated with BS. Eleven patients had single point mutations, one patient had a deletion (1380 del N) and one patient had a mutation within the splicing junction (IVS21+1 g&gt;a). The whole-cell patch clamp technique revealed that four novel mutations (F532C, R814Q, G833R, R878C) showed loss of function, and peak INa of a novel SNP (L1988R) transiently expressed in HEK 293 cells was significantly reduced (P&lt;0.05). RT-PCR analysis revealed that the intronic mutation (IVS21+1 g&gt;a) resulted in exon 21 deletion of SCN5A in cardiac biopsy specimens from the patient (Figure ). Conclusions: We detected five novel SCN5A mutations (1380 del N, F532C, R814Q, G833R, R878C) and a novel disease-associated SNP (L1988R) in patients with BS. We showed a novel analysis of splicing mutation (IVS21+1 g&gt;a) that resulted in exon skipping in the heart.
Traité d'Urologie.
Journal: JAMA (1922)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Increased neutrophil function induced by bile duct ligation in a rat model
Authors: R Levy
Journal: Hepatology (1993)

Neutrophil function was studied in rats with common bile duct ligation. Superoxide production stimulated by phorhol myristate acetate, opsonized zymosan or formyl-methionyl-leucyl-phenylalanine; phagocytosis; and chemotaxis were significantly greater in neutrophils from rats with common bile duct ligation than in sham-operated control rats. Enhanced neutrophil activity was observed within 12 hr of bile duct ligation; it remained increased during the 15-day study. Preincubation of neutrophils from control rats with sera of rats with common bile duct ligation did not increase superoxide generation. This suggests that the high superoxide production observed in neutrophils of rats with common bile duct ligation was not an immediate effect of the serum. Neutrophils of rats with portal vein ligation exhibited normal activity, indicating that portal systemic shunting per se is not the underlying mechanism for increased activity. The elevated levels of AST and alkaline phosphatase, indicating liver damage, that appeared within 12 hr of bile duct ligation correlated with the increased superoxide generation. (HEPATOLOGY 1993;17:908–914.)
Physiological and Hemodynamic Evaluation of Nonuniform Direct Cardiac Compression
Authors: John H. Artrip, Geng-Hua Yi, Howard R. Levin, Daniel Burkhoff, Jie Wang
Journal: Circulation (1999)

Background —Biventricular direct cardiac compression (DCC) has the potential to support the failing heart without the complications associated with a blood/device interface encountered with the use of current ventricular assist devices. A clinically designed DCC device that provides compression pressure around the base of the heart in synchrony with native ventricular contractions was evaluated with the use of an ex vivo and in vivo canine model of heart failure. Methods and Results —The device was tested over a series of ventricular preloads with the use of an ex vivo canine heart preparation and computerized afterload system that mimicked the conditions of heart failure. The end-systolic pressure-volume relation of the left and right ventricles was shifted upward in parallel by DCC, with the magnitude of the shift averaging 40% of the device compression pressure. The device was tested in vivo with the use of a canine model of acute ischemic heart failure in which graded reductions in ventricular function were created through serial coronary artery embolizations. Under the most severe condition of heart failure, DCC improved cardiac output (CO) by 104% (0.80±0.33 to 1.63±0.40 L/min) and mean arterial pressure by 95% (45.6±11 to 89.0±18.2 mm Hg). The CO was typically restored to ≈60% of the normal baseline value, despite attempts to further increase CO by increasing the amount or duration of compression pressure. Conclusions —Nonuniform DCC significantly improves the left and right ventricular pressure-generating capability and, in the setting of acute heart failure, can increase CO and mean arterial pressure. Such DCC devices can potentially avoid the complications associated with currently available ventricular support devices that involve a blood/device interface.
Authors' response
Authors: N. M. Probst-Hensch, I. Curjuric, P.-O. Bridevaux, N. Kunzli, C. Schindler, T. Rochat
Journal: Thorax (2010)

<h3>Objective:</h3> Alemtuzumab is a monoclonal antibody that targets the CD52 protein expressed on T and B lymphocytes. This treatment may result in severe adverse events such as allergic reactions, de novo autoimmune diseases, opportunistic infections, and stroke. In this report, we described a relapsing-remitting multiple sclerosis (RRMS) patient without any risk factors for cerebrovascular disease who had a hemorrhagic stroke during the second course of alemtuzumab treatment. <h3>Background:</h3> NA <h3>Design/Methods:</h3> NA <h3>Results:</h3> Herein, we report a 52-years-old female patient with RRMS that was diagnosed 30 years ago. During the long course of the disease, she received interferons, azathioprine, fingolimod, and natalizumab. Her treatment was switched to alemtuzumab one year ago due to the inefficacy of natalizumab. The patient experienced no severe side effects except headache and nausea during the first course of the treatment, and her clinical course was stable for one year. Her EDSS was 5.0 when she was admitted for administration of the second course of alemtuzumab. On the third day of treatment, she complained of headache and hypertension (170/100) that was treated with analgesics and ramipril 2,5 mg. Four hours after infusion of the third dose, the patient had an acute loss of consciousness and left hemiplegia. Her brain computed tomography revealed a massive (66x44 mm) right putaminal hemorrhage. The patient underwent an urgent hematoma evacuation craniotomy with external ventricular drainage. One day after the surgery, the patient developed another hematoma in the left putamen when she was normotensive without apparent hematological abnormalities. <h3>Conclusions:</h3> To date, only five cases with intracerebral hemorrhage associated with alemtuzumab treatment were reported. Previous reports blamed elevated blood pressure as a possible culprit in the cerebral hemorrhage. The occurrence of secondary putaminal hemorrhage when the patient was normotensive contradicts this hypothesis. This case reveals the need for further investigation of possible endothelial damage due to alemtuzumab treatment. <b>Disclosure:</b> Dr. Inci has nothing to disclose. Dr. Gunduz has nothing to disclose. Dr. Kurtuncu has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Merck%2C%20Novartis%2C%20Teva%2C%20Genzyme%2C%20Bayer%2C%20Roche. Dr. Eraksoy has nothing to disclose.
New Tool in Epidemiology
Journal: JAMA (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 3390: Marginal Overlap between Electrocardiographic Abnormalities in Patients with Hypertrophic Cardiomyopathy and Trained Athletes: Implications for Preparticipation Screening
Authors: Paola Melacini, Cinzia Cianfrocca, Chiara Calore, Francesca Bovolato, Fernando Di Paolo, Filippo Quattrini, Francesco Pelliccia, Sanjay Sharma, William J McKenna, Barry J Maron, Antonio Pelliccia, Domenico Corrado
Journal: Circulation (2007)

Background: Hypertrophic cardiomyopathy (HCM) is usually associated with ECG abnormalities such as left ventricular hypertrophy (LVH), repolarization changes, and pathologic Q waves; instead, physiologic hypertrophy in trained athletes manifests as an isolated increase of QRS amplitude. We assessed whether the ECG pattern of pathologic hypertrophy of HCM overlaps with that of physiologic hypertrophy of athlete’s heart, particularly by evaluating what proportion of individuals from both groups had pure QRS voltage criteria (Sokolow-Lyon) for LVH. Methods: Using accepted diagnostic criteria, we examined and compared the ECG tracings of 260 consecutive patients with clinical and echocardiographic diagnosis of HCM and those of 1005 trained athletes undergoing preparticipation cardiovascular evaluation, including ECG and echocardiography. Results: An abnormal ECG was found in 246 of 260 (94.6%) patients with HCM and in 817 of 1005 athletes (81.3%). The majority of patients with HCM had one or more of the following ECG changes: repolarization ST/T abnormalities in 209 (80%), pathologic Q waves (Q waves ≥0.04 s in duration or ≥25% of the height of the ensuing R wave) in 103 (39.6%); left atrial enlargement in 75 (28.8%), intraventricular conduction abnormalities (QRS duration ≥90 ms) in 71 (27.3%) and left axis deviation in 9 (3.5%). ECG tracings showed isolated increase of QRS voltages in 5 HCM patients (1.9%) and were completely normal in 14 (5.4%). Compared with patients with HCM, trained athletes significantly more often had isolated voltage criteria for LVH (403, 40%; p&lt;0.0001), but less often showed negative T waves (27, 2.7%; p&lt;0.0001), pathologic Q waves (17, 1.7%; p&lt;0.0001), and nonvoltage criteria of LVH (13, 1.3%; p&lt;0.0001). No athletes with isolated voltage criteria had echocardiographic evidence of HCM. Conclusions: ECG in HCM overlaps marginally with ECG findings in trained athletes. An isolated increase of QRS voltage is an unusual pattern (1.9%) of LVH in patients with HCM, while is frequently observed in trained athletes. Systematic echocardiographic evaluation of athletes fulfilling isolated QRS voltage criteria at preparticipation screening is not justified, resulting in a considerable cost savings.
THE NATIONAL HALOTHANE STUDY
Journal: JAMA (1966)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Drugs Evaluated by the Council on Drugs
Journal: JAMA (1963)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Role of heparin-binding epidermal growth factor?like growth factor as a hepatotrophic factor in rat liver regeneration after partial hepatectomy
Authors: S KISO
Journal: Hepatology (1995)

Several growth factors including hepatocyte growth factor (HGF) have been implicated in the regulation of liver regeneration. Recently, we reported that heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) has hepatotrophic effects in vitro. We investigated the role of HB-EGF as a hepatotrophic factor in regenerating rat liver after 70% partial hepatectomy. The level of HB-EGF messenger RNA (mRNA) in regenerating rat liver increased 1.5 hours after partial hepatectomy and reached a maximum (about sevenfold over normal) at 6 hours. In contrast, hepatic HGF mRNA levels increased at 12 hours and achieved maximal expression at 24 hours. HB-EGF protein expression increased about 2.8-fold over normal at 10 hours after partial hepatectomy. The number of EGF receptors, to which HB-EGF binds, decreased 6 hours after partial hepatectomy. HB-EGF mRNA levels increased in nonparenchymal cells (NPCs) at 6 hours after partial hepatectomy but not in hepatocytes. Using the reverse transcription-polymerase chain reaction (RT-PCR), HB-EGF gene expression was increased predominantly in Kupffer cells and sinusoidal endothelial cells but not in lipocytes and hepatocytes. These results indicated that HB-EGF may be an important growth factor, produced in an earlier phase rather than HGF, in the regenerating liver after partial hepatectomy by a paracrine mechanism.
Transactions of the Medical Society of the State of Pennsylvania at its forty-sixth annual session, held at Harrisburg, 1896. Vol. XXVII.
Journal: JAMA (1896)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Mortality of employees of the United Kingdom Atomic Energy Authority, 1946-1979.
Authors: V Beral, H Inskip, P Fraser, M Booth, D Coleman, G Rose
Journal: BMJ (1985)

An analysis was conducted of 3373 deaths among 39 546 people employed by the United Kingdom Atomic Energy Authority between 1946 and 1979, the population having been followed up for an average of 16 years. Overall the death rates were below those prevailing in England and Wales but consistent with those expected in a normal workforce. At ages 15-74 years the standardised mortality ratios (SMRs) were 74 for deaths from all causes and 79 for deaths from all cancers. Mortality from only four causes was above the national average--namely, testicular cancer (SMR 153; 10 deaths), leukaemia (SMR 123; 35 deaths), thyroid cancer (SMR 122; three deaths), non-Hodgkin9s lymphoma (SMR 107; 20 deaths)--but in none was the increase significant at the 5% level. Half of the authority9s employees were recorded as having been monitored for exposure to radiation, their collective recorded exposure being 660 Sv (65 954 rem). Among these prostatic cancer was the only condition with a clearly increased mortality in relation to exposure. Of the 19 men who had a radiation record and died from prostatic cancer at ages 15-74 years, nine had been monitored for several different sources of exposure to radiation. The standardised mortality ratios were 889 (six deaths) in employees monitored for contamination by tritium, 254 (nine deaths) in those monitored for contamination by other radionuclides, and 385 (nine deaths) in those with dosimeter readings totalling more than 50 mSv (5 rem); but the same nine subjects tended to account for each of these significantly raised ratios. Because multiple exposures were common and other relevant information was not available the reason for the increased mortality from prostatic cancer in this population could not be determined and requires further investigation. Excess mortality rates of 2.2 and 12.5 deaths per million person years per 10 mSv (1 rem) were estimated for leukaemia and all cancers, respectively. The confidence limits around these estimates were wide, included zero, and made it unlikely that the International Commission on Radiological Protection9s cancer risk coefficients were underestimated by more than 15-fold. Thus despite this being the largest British workforce whose mortality has been reported in relation to low level ionising radiation exposure, even larger populations will need to be followed up over longer periods before narrower ranges of risk estimates can be derived.
OA01.01 Pembrolizumab Plus Chemotherapy for Advanced NSCLC without Tumor PD-L1 Expression: Pooled Analysis of KN021G, KN189 and KN407
Authors: H. Borghaei, C. Langer, L. Paz-Ares, D. Rodriguez-Abreu, V. Papadimitrakopoulou, M. Garassino, B. Houghton, T. Kurata, Y. Cheng, J. Lin, C. Pietanza, B. Piperdi, S. Gadgeel
Journal: Journal of Thoracic Oncology (2019)
Thorotrast
Authors: R. H. Carrigan
Journal: JAMA (1966)

<h3>To the Editor:—</h3> The suggestion of Paul H. Blachly, MD, regarding computer recording of automobile accident data (<b>197</b>:930, 1966) is a good one, but I would like to suggest that it does not go far enough. Computer capacity could easily handle data on the other extremely important items involved in automobile accidents, not included in Dr. Blachly's suggestion. The object, of course, would be to use the stored data to minimize accidents. There is no question that automobile safety can be improved, but recent publicity has caused many of us to overlook the driver or the road. Whenever I read in the paper that such and such occurred and so and so was killed I always remain curious as to why one car or the other was where it was when it shouldn't have been (whether a one-car or a multiple-car accident). Was a curve inadequately marked by the